The present invention pertains to the field of apparatus for treatment of a failing heart. In particular, the apparatus and its related methods of the present invention is directed toward reducing the wall stress in the failing heart. The present invention further includes methods and devices for improving cardiac function in hearts having discrete zones of infarcted tissue. Such methods and devices reduce the radius of curvature and/or alter the geometry or shape of the infarcted tissue and adjacent regions to thereby reduce wall stress on the heart it and improve the heart""s pumping performance.
The syndrome of heart failure is a common course for the progression of many forms of heart disease. Heart failure may be considered to be the condition in which an abnormality of cardiac function is responsible for the inability of the heart to pump blood at a rate commensurate with the requirements of the metabolizing tissues, or can do so only at an abnormally elevated filling pressure. There are many specific disease processes that can lead to heart failure. Typically these processes result in dilatation of the left ventricular chamber. Etiologies that can lead to this form of failure include idiopathic, valvular, viral, and ischemic cardiomyopathies.
The process of ventricular dilatation is generally the result of chronic volume overload or specific damage to the myocardium. In a normal heart that is exposed to long term increased cardiac output requirements, for example, that of an athlete, there is an adaptive process of slight ventricular dilation and muscle myocyte hypertrophy. In this way, the heart fully compensates for the increased cardiac output requirements. With damage to the myocardium or chronic volume overload, however, there are increased requirements put on the contracting myocardium to such a level that this compensated state is never achieved and the heart continues to dilate.
The basic problem with a large dilated left ventricle is that there is a significant increase in wall tension and/or stress both during diastolic filling and during systolic contraction. In a normal heart, the adaptation of muscle hypertrophy (thickening) and ventricular dilatation maintain a fairly constant wall tension for systolic contraction. However, in a failing heart, the ongoing dilatation is greater than the hypertrophy and the result is a rising wall tension requirement for systolic contraction. This is felt to be an ongoing insult to the muscle myocyte resulting in further muscle damage. The increase in wall stress is also true for diastolic filling. Additionally, because of the lack of cardiac output, there is generally a rise in ventricular filling pressure from several physiologic mechanisms. Moreover, in diastole there is both a diameter increase and a pressure increase over normal, both contributing to higher wall stress levels. The increase in diastolic wall stress is felt to be the primary contributor to ongoing dilatation of the chamber.
Prior treatments for heart failure associated with such dilatation fall into three general categories. The first being pharmacological, for example, diuretics and ACE inhibitors. The second being assist systems, for example, pumps. Finally, surgical treatments have been experimented with, which are described in more detail below.
With respect to pharmacological treatments, diuretics have been used to reduce the workload of the heart by reducing blood volume and preload. Clinically, preload is defined in several ways including left ventricular end diastolic pressure (LVEDP), or indirectly by left ventricular end diastolic volume (LVEDV). Physiologically, the preferred definition is the length of stretch of the sarcomere at end diastole. Diuretics reduce extra cellular fluid which builds in congestive heart failure patients increasing preload conditions. Nitrates, arteriolar vasodilators, angiotensin converting enzyme (ACE) inhibitors have been used to treat heart failure through the reduction of cardiac workload by reducing afterload. Afterload may be defined as the tension or stress required in the wall of the ventricle during ejection. Inotropes function to increase cardiac output by increasing the force and speed of cardiac muscle contraction. These drug therapies offer some beneficial effects but do not stop the progression of the disease.
Assist devices include mechanical pumps. Mechanical pumps reduce the load on the heart by performing all or part of the pumping function normally done by the heart. Currently, mechanical pumps are used to sustain the patient while a donor heart for transplantation becomes available for the patient.
There are at least four surgical procedures for treatment of heart failure associated with dilatation: 1) heart transplantation; 2) dynamic cardiomyoplasty; 3) the Batista partial left ventriculectomy; and 4) the Jatene and Dor procedures for ischemic cardiomyopathy, discussed in more detail below. Heart transplantation has serious limitations including restricted availability of organs and adverse effects of immunosuppressive therapies required following heart transplantation. Cardiomyoplasty involves wrapping the heart with skeletal muscle and electrically stimulating the muscle to contract synchronously with the heart in order to help the pumping function of the heart. The Batista partial left ventriculectomy surgically remodels the left ventricle by removing a segment of the muscular wall. This procedure reduces the diameter of the dilated heart, which in turn reduces the loading of the heart. However, this extremely invasive procedure reduces muscle mass of the heart.
One form of heart failure, ischemic cardiomyopathy, results from the formation of one or more zones of ischemia, or infarction, of the myocardium. Infarction occurs when blood supply to the heart tissue has been obstructed resulting in a region of tissue that loses its ability to contract (referred to as infarcted tissue). The presence of infarcted tissue may lead to three conditions in the heart causing cardiac malfunction. These conditions are ventricular aneurysms (ventricular dyskinesia), non-aneurysmal ischemic or infarcted myocardium (ventricular akinesia), and mitral regurgitation.
Ventricular aneurysms typically result from a transmural myocardial infarction, frequently due to the occlusion of the left anterior descending artery (LAD). This results in a transmural infarcted region of the apical portion of the left ventricle and anterior septal. A ventricular aneurysm is formed when the infarction weakens the heart wall to such an extent that the tissue stretches and thins, causing the left ventricular wall to expand during systole (dyskinesia). FIG. 55 illustrates a ventricular aneurysm A occurring in the apical region of left ventricle LV. As shown by the shaded region in FIG. 55, aneurysm A includes infarcted tissue 24 that results in a reduced wall thickness when compared to adjacent non-infarcted wall regions, as shown by the unshaded regions in FIG. 55. FIG. 55 also shows the septal wall S partially infarcted, again shown by the shaded region. The ventricular aneurysm also may be dyskinetic, meaning that when the ventricle contracts, the aneurysm further dilates, or bulges, outward. The infarcted region of the septal wall S also may be particularly dyskinetic, especially in the case of the infarcted tissue having progressed to an aneurysm.
The bulge resulting from an aneurysm can have several serious effects on the heart and its performance that can lead to in both morbidity and mortality. For example, because the bulge creates a geometric abnormality as well as a region of non-contracting tissue, thrombosis is more likely to occur in that region. Thrombosis is the formation of a blood clot, or thrombus, that can cause other medical complications, such as a stroke. An ischemic stroke is a blockage of blood flow to the brain that occurs when the thrombus breaks free and is ejected out of the ventricle.
Another serious effect this bulging can have is the denigration of the heart""s pumping function. The aneurysmal bulge creates problems with pumping function in at least three ways. First, the infarcted tissue does not contribute to the pumping of the ventricle because it does not contract (akinesia). To account for this loss of pumping, remaining portions of the ventricle wall may contract more to maintain cardiac output. If the infarcted region thins and progresses to an aneurysm (dyskinesia), this effect is further exacerbated by the aneurysm expanding with a portion of the blood from the ventricular contraction. This further increases the contractile requirement of the remaining functional myocardium.
Second, the aneurysmal bulge alters the geometry of the entire ventricular chamber. Thus the ventricle develops a larger radius of curvature, which directly applies more tension to the heart wall, as characterized by LaPlace""s law.
Third, over time, the above two conditions lead the functional muscle of the ventricle to work harder than normal. This can lead to continued dilatation of the ventricle, increasing tension in the walls of the heart, with increased myocardial oxygen requirement and further progressing heart failure.
Non-aneurysmal ischemic or infarcted myocardium (akinesia) occurs when a major coronary artery is occluded and results in infarction in the myocardial tissue, but without a bulging aneurysm. In a manner similar to an aneurysm, the akinetic ischemic or infarcted zone ceases to participate in the ventricular contraction. This results in the functioning, contractile myocardium needing to contract more to make up for the lack of contraction of the akinetic zone. Typically, the result is the entire ventricle increasing in size, which increases wall stress. Again, since the functioning myocardium must work harder, continuing progression of heart failure can occur.
Mitral regurgitation also may result from infarcted tissue, depending on the region of the ventricle that has become infarcted or aneurysmal and any subsequent overall ventricular dilation. Mitral regurgitation is a condition whereby blood leaks through the mitral valve due to an improper positioning of the valve structures that causes it not to close entirely. If the infarcted or aneurysmal region is located in the vicinity of the mitral valve, geometric abnormalities may cause the mitral valve to alter its normal position and dimension, and may lead to annular dilatation and the development of mitral regurgitation.
Typical treatments of infarcted tissue, and ventricular aneurysms in particular, include a variety of open surgical procedures. In the case of a ventricular aneurysm, traditionally, a xe2x80x9clinearxe2x80x9d aneurysmectomy is performed. This procedure involves the removal of aneurysmal portions of the anterior wall along with any thrombus that may exist. FIG. 41 illustrates the result of a conventional surgical method when an aneurysm occurs in the distal left ventricle. According to this method, the region of aneurysmal scar tissue that extends through the entire thickness of the chamber wall (transmural infarction) is removed by incision and the remaining border zone regions 24xe2x80x2 (i.e., regions where infarcted tissue meets non-infarcted muscle) are sewn together with a suture 27. In a linear aneurysm repair procedure, the ventricular septal wall S that is infarcted is left untouched. Additionally, the septal wall generally remains untouched because simple excision and suturing does not involve excluding or cutting the septal wall. Usually, only those wall portions having infarcted tissue through their thickness (transmural infarcted) are removed while the portions having infarcted tissue only on an inner wall (endocardial infarcted) are left in place. The term border zone refers to this region of endocardial infarction. This surgical procedure results in some infarcted tissue regions remaining in the heart chamber, particularly any infarcted tissue in the septal wall. The effects of the remaining non-contractile tissue stresses the remaining contractile tissue because this contractile tissue must xe2x80x9cmake upxe2x80x9d for the non-contracting and often dyskinetic tissue. Over time, these effects can continue to lead to progression of heart failure.
These procedures have to be performed with the patient on cardiopulmonary bypass. The heart also may be stopped in order to perform the surgery. Any thrombus inside the ventricle is removed. Clinical results of this traditional surgical procedure have been mixed with respect to improvement in cardiac function.
Newer surgical approaches include the xe2x80x9cDorxe2x80x9d and xe2x80x9cJatenexe2x80x9d procedures. In the xe2x80x9cDorxe2x80x9d procedure, the aneurysm is removed and an endocardial patch is placed to cover the dyskinetic septal wall portion of the aneurysm. In this manner, at least the portion of stroke volume xe2x80x9clostxe2x80x9d to dyskinesia is restored. In the xe2x80x9cJatenexe2x80x9d technique, a purse string suture is placed at the base of the aneurysm. The infarcted septal wall is circumferentially reduced by inbrication with sutures. The result is that most of the aneurysmal tissue is excluded from the ventricle. These procedures address the infarcted septal wall, generally left untouched in the traditional linear aneurysmectomy, by either exclusion or by the use of a surgical patch. These newer techniques are also used in cases of non-aneurysmal infarctions (akinesia). In these cases, the exclusion or elimination of the infarcted region reduces the size and therefore the radius of the chamber, thereby lowering wall stress.
These various described techniques for treating infarcted and aneurysmal tissue regions in the heart wall suffer from limitations and drawbacks. For instance, many of the surgical techniques involve invasive incisions in the heart wall which can be traumatic and risky to patients. Also, while these procedures attempt to improve cardiac function by removal of the aneurysm or infarcted tissue, they only minimally reduce the wall stress of the remaining contractile ventricle. Furthermore, patients typically undergo cardiopulmonary bypass and/or their heart is stopped during many of these surgeries.
The advantages and purpose of the invention will be set forth in part in the description which follows, and in part will be obvious from the description, or may be learned by practice of the invention. The advantages and purpose of the invention will be realized and attained by means of the elements and combinations particularly pointed out in the appended claims.
Due to the drawbacks and limitations of the previous techniques for treating dilated, infarcted, and aneurysmal tissue in hearts, there exists a need for alternative methods and devices that are less invasive, pose less risk to the patient, and are likely to prove more clinically effective. The present invention provides improvements in these areas over the existing techniques.
One aspect of the present invention pertains to a non-pharmacological, passive apparatus and method for the treatment of a failing heart due to dilatation. The device is configured to reduce the tension in the heart wall. It is believed to reverse, stop or slow the disease process of a failing heart as it reduces the energy consumption of the failing heart, decreases isovolumetric contraction, increases isotonic contraction (sarcomere shortening), which in turn increases stroke volume. The device reduces wall tension during diastole and systole.
These apparatus of the present invention which reduce heart wall stress by changing chamber wall geometry can be referred to as xe2x80x9csplintsxe2x80x9d. Splints can be grouped as either xe2x80x9cfull cycle splints,xe2x80x9d which engage the heart to produce a chamber shape change throughout the cardiac cycle, or xe2x80x9crestrictive splints,xe2x80x9d which do not engage the heart wall at end systole to produce a chamber shape change.
In one embodiment, the apparatus includes a tension member for drawing at least two walls of the heart chamber toward each other to reduce the radius or area of the heart chamber in at least one cross sectional plane. The tension member has anchoring members disposed at opposite ends for engagement with the heart or chamber wall.
In another embodiment, the apparatus includes a compression member for drawing at least two walls of a heart chamber toward each other. In one embodiment, the compression member includes a balloon. In another embodiment of the apparatus, a frame is provided for supporting the compression member.
Yet another embodiment of the invention includes a clamp having two ends biased toward one another for drawing at least two walls of a heart chamber toward each other. The clamp includes at least two ends having atraumatic anchoring members disposed thereon for engagement with the heart or chamber wall.
In yet another embodiment, a heart wall tension reduction apparatus is provided which includes a first tension member having two oppositely disposed ends and first and second elongate anchor members. A second tension member can be provided. One of the elongate anchors may be substituted for by two smaller anchors.
In an alternate embodiment of the heart wall tension reduction apparatus, an elongate compression member can be provided. First and second elongate lever members preferably extend from opposite ends of the compression member. A tension member extends between the first and second lever members.
The compression member of the above embodiment can be disposed exterior to, or internally of the heart. The tension member extends through the chamber or chambers to bias the lever members toward the heart.
In yet another embodiment of a heart wall tension reduction apparatus in accordance with the present invention, a rigid elongate frame member is provided. The frame member can extend through one or more chambers of the heart. One or more cantilever members can be disposed at opposite ends of the frame member. Each cantilever member includes at least one atraumatic pad disposed thereon. The atraumatic pads disposed at opposite ends of the frame member can be biased toward each other to compress the heart chamber.
One method of placing a heart wall tension apparatus or splint on a human heart includes the step of extending a hollow needle through at least one chamber of the heart such that each end of the needle is external to the chamber. A flexible leader is connected to a first end of a tension member. A second end of the tension member is connected to an atraumatic pad. The leader is advanced through the needle from one end of the needle to the other. The leader is further advanced until the second end of the tension member is proximate the heart and the first end of the tension member is external to the heart. A second atraumatic pad is connected to the first end of the tension member such that the first and second atraumatic pads engage the heart.
Yet another method of placing a heart wall tension apparatus on a heart includes the step of extending a needle having a flexible tension member releasably connected thereto through at least one chamber of the heart such that opposite ends of the tension member are external to the chamber and exposed on opposite sides of the chamber. The needle is removed from the tension member. Then first and second atraumatic pads are connected to the tension member at opposite ends of the tension member.
In the treatment of heart failure due to infarcted tissue, possibly including an aneurysm as well, another aspect of the invention involves placing the splint relative to the infarcted or aneurysmal zone, and, in a preferred embodiment, diametrically across the infarcted or aneurysmal zone, to decrease the stress on the infarcted tissue and adjacent border zone tissue. An alternative to diametric placement of the splint includes placing one atraumatic anchor member of the splint at the center of the infarcted or aneurysmal region, extending the splint across the entire heart chamber, and placing the second atraumatic anchor member on the opposite chamber wall. In the case of infarcted or aneurysmal tissue in the vicinity of the mitral valve, an aspect of the present invention includes a method of placing the splint adjacent but below the mitral valve to draw the papillary muscles together or the walls of the valve seat together. It is also envisioned to use the splint both as the sole device for treating infarcted tissue and aneurysms or in combination with the surgical techniques described earlier.
An external splint, using a compression member, also may be used to treat a heart having infarcted or aneurysmal tissue. The compression member is placed entirely exterior to the heart and positioned so as to result in similar effects as discussed above with reference to the splint.
Other inventive methods and devices to treat infarcted tissue and aneurysms include a variety of patching and suturing methods and related devices. Each of these methods and related devices reduces the radius of curvature of the infarcted wall region and adjacent regions and contains the infarcted region to stop further progression.
A further aspect of the invention involves the identification of aneurysmal and infarcted regions using any one or more of a variety of devices and methods. These devices and methods, which will be described more specifically herein, include a bipolar electrode, liquid dye injection and tracing, fiber optics, MRI, and ultrasound. These devices can be used to distinguish between healthy and infarcted heart tissue.
In accordance with the purposes of the invention as embodied and broadly described herein, methods and related devices for treating a heart having infarcted tissue in one of its chambers are disclosed. In a preferred embodiment of the invention, a method for treating a heart having a zone of infarcted tissue in its chamber includes deforming a wall of the chamber that includes the infarcted tissue such that a radius of curvature of the wall is reduced.
In another preferred embodiment of the present invention, the method involves providing at least one tension member having two ends and an anchor on each end. The tension member is positioned transverse to the chamber to reduce the radius of curvature of the wall of the chamber that includes the infarcted tissue and/or to draw the walls containing the infarcted tissue together.
In another preferred embodiment, the present invention involves positioning a tension member having anchors on each of its ends transverse to the heart chamber so that the infarcted tissue is drawn toward an interior of the heart chamber. The anchors are placed exterior to the chamber.
In yet another preferred embodiment, the present invention includes positioning a compression member having a first end and a second end, each having anchor members around an exterior of the heart. The compression member is positioned so as to surround the chamber with infarcted tissue and to reduce the radius of curvature of the portion of the heart wall that has the infarcted tissue.
In accordance with another preferred embodiment, a method of treating a heart having infarcted tissue in one of its chambers involves epicardial suturing around the perimeter of a region of infarcted tissue and pulling free ends of the suture to draw the infarcted tissue region together. The suture is then secured to hold the infarcted tissue together. This suture also may be employed in combination with a myocardial patch or a substantially rigid enclosure member, both of which represent other preferred embodiments of the present invention.
In accordance with another preferred embodiment of the present invention, a method of treating a heart having infarcted tissue in one of its chambers involves positioning an enclosure member around a zone of infarcted tissue. During the positioning, the enclosure member has a first configuration. After positioning, the enclosure member is then secured to a wall of the heart and the enclosure member reconfigures to a second configuration. Upon reconfiguration to the second configuration, the radius of curvature of the portion of the heart wall including the infarcted tissue reduces.
In accordance with yet another preferred embodiment of the present invention, an apparatus for treating a heart having a zone of infarcted tissue in one of its chambers is provided. The apparatus includes an enclosure member adapted to assume a first configuration during placement of the enclosure member around an infarcted tissue zone. The enclosure member further is adapted to assume a second configuration after securing the enclosure member to a heart wall surrounding the chamber. The second configuration draws the infarcted tissue toward a center of the enclosure member and reduces the radius of curvature of the heart wall.
In accordance with another preferred embodiment of the present invention, a device for treating a heart having infarcted tissue in one of its chambers is provided. The device includes a patch adapted to be attached to the heart, with a substantially elongated member secured to the patch. When the patch is placed over the infarcted or aneurysmal tissue region, the elongated member tends to push the infarcted tissue region toward an interior of the heart chamber.
In accordance with yet another preferred embodiment of the present invention, a plurality of sutures are attached at one end to points on a chamber wall proximate to an infarcted tissue region and the sutures are extended up through a space defined by an enclosure member to draw the infarcted tissue together and through the enclosure member. The other ends of the sutures are then attached to points on the wall of the chamber to hold the tissue in place.
It is to be understood that both the foregoing general description and the following detailed description are exemplary and explanatory only and are not restrictive of the invention, as claimed.